PUD & GERD Flashcards

1
Q

GASTROINTESTINAL DRUGS

A

The neural pathway delivers acetylcholine which is released from
postganglionic nerve terminals.
Gastrin is released from antral G-cells located in the antrum and
duodenum and delivered to the parietal cell via the systemic
circulation.
Histamine is released from mucosal mast cells into the interstitial
fluid via the paracrine pathway.
Pepsinogen is a proenzyme that will form pepsin in an acidic
environment, and it combines with acid to form a proteolytic
complex that further aids in the digestive process.

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2
Q

Histamine H2 receptor antagonists drugs & use

A

cimetidine + tidine
peptic ulcers: all four drugs are equally effective in promoting healing of gastric and duodenal ulcers and provide an overall healing rate of 70-95%; without concurrent H. Pylori eradication treatment, there is a high risk of recurrence of the ulcer (60-100% of cases)
ii. GERD

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3
Q

Histamine H2 receptor antagonists moa & pharmacokinetics

A

these drugs block the actions of histamine on histamine H2 receptors; in the stomach they
inhibit gastric acid secretion
induced by histamine, and to a lesser extent inhibit gastrin and muscarinic receptor
stimulated acid secretion

all given orally; nizatidine has a higher bioavailability (about 90%) than the others (about 50%)
because nizatidine does not undergo much first-pass
metabolism; potency of the drugs is famotidine > ranitidine = nizatidine >
cimetidine

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4
Q

Histamine H2 receptor antagonists adverse effects

A

limited CNS effects; since cimetidine inhibits P450 enzymes it can slow metabolism and potentiate the action of several drugs (ex: warfarin, diazepam, phenytoin, quinidine, carbamazepine, theophylline, imipramine); also, cimetidine may have antiandrogenic effects which may lead to gynecomastia (also a P450 effect); overall incidence of side effects is low due to limited function of H2 receptors in other tissues; headache, dizziness, and nausea have been observed

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5
Q

Inhibitors of the H+ /K+ –ATPase proton pump

drugs & use

A

omeprazole, lansoprazole, rabeprazole, pantoprazole,
esomeprazole (S-isomer of omeprazole)

therapeutic use: treatment of active ulcers; reflux
esophagitis; long-term treatment of hypersecretory conditions
(Zollinger-Ellison); in combination with antimicrobial agents
to eradicate H. Pylori

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6
Q

Inhibitors of the H+ /K+ –ATPase proton pump moa & kinetics

A

inhibit gastric acid secretion by
irreversibly blocking the proton pump; since the action of the
drugs is irreversible, the inhibition of gastric acid secretion
lasts long after the drug has been eliminated
All PPIs are prodrugs
and must be converted
to the active form. Irreversible covalent bond

given orally as delayed-release capsules
(Note: these drugs are stable at neutral pH but are destroyed
by gastric acid; therefore, if the gelatin-coated capsule is
broken prior to swallowing the drug will be destroyed; if
taken properly, the drug will be released from the capsule in
the intestine where it is rapidly absorbed); omeprazole,
inhibits P450 enzymes and can affect metabolism of warfarin, phenytoin, diazepam, and cyclosporine

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7
Q

Inhibitors of the H+ /K+ –ATPase proton pump adverse effects

A

well-tolerated; about 3% of patients experience GI effects such as nausea, diarrhea, and abdominal colic; do not use with clopidogrel (effect)

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8
Q

Eradication of H. Pylori

A

a. combination therapy is used: PPI + 2 antibiotics

b. therapeutic use: eradicates H. Pylori in 90% of
patients to aid in ulcer treatment

c. mechanism of action: kills the bacteria (see mechanisms
for metronidazole, clarithromycin, amoxicillin, tetracycline)
MCAT

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9
Q

Prostaglandins drugs & use

A

misoprostol
prevent gastric ulcers caused by NSAIDs;
less effective than the H2 receptor antagonists in treating
peptic ulcers; available in combination with diclofenac
(Arthrotec)

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10
Q

Prostaglandins moa & adverse

A

mechanism of action: is a prostaglandin E2 and I2 receptor
agonist so it will decrease cAMP levels and inhibit acid; stimulates mucous and bicarbonate production

adverse effects: diarrhea, abdominal cramping; abortion, premature birth, birth defects (cat. X)

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11
Q

Antimuscarinic agents

A

hyoscyamine, dicyclomine, glycopyrrolate

therapeutic use: adjuncts in peptic ulcer treatment

mechanism of action: block muscarinic receptors which
inhibits gastric acid secretion

adverse effects: atropine-like (limits use of these drugs)

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12
Q

Antacids

A

aluminum hydroxides and magnesium hydroxides, calcium
carbonates (Tums, Rolaids); sodium bicarbonate; Al(OH)3 +
Mg(OH)2 + alginic acid (Gaviscon)

therapeutic use: promote healing of gastric ulcers; relieve
symptoms of GERD

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13
Q

antacids moa

A

the antacids react with gastric acid
to produce water and a salt; antacids also reduce pepsin
activity by increasing the pH (pepsin activity decreases
as pH increases); Gaviscon is not as effective as the others
at neutralizing acid but does form a highly viscous
solution which acts as a mechanical barrier to reflux and
protects the mucosa

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14
Q

antacids adverse

A

aluminum hydroxide may cause
constipation; magnesium hydroxide may cause diarrhea; bicarbonates have the potential to cause systemic alkalosis, liberate CO2 which causes belching and flatulence; the sodium content of antacids is important in patients with hypertension of congestive heart failure

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15
Q

antacids drug interactions

A

it is advisable to avoid concurrent
administration of antacids and other drugs since antacids can
affect absorption; sodium bicarbonate is used to alkalinize
the urine
Take antacids 2 hours before or after other drugs

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16
Q

Mucosal protective agents

A

sucralfate

colloidal bismuth

17
Q

sucralfate

A

is a complex of aluminum hydroxide and
sulfated sucrose that binds to positively charged groups in
proteins of the mucosa; sucralfate creates a physical barrier
that impairs diffusion of HCl and prevents degradation of the
mucosa by pepsin; it also stimulates prostaglandin release and
mucus and bicarbonate output and is beneficial in PUD;
sucralfate requires an acidic environment to be activated,
the drug should not be used together with antacids

18
Q

colloidal bismuth

A

can neutralize gastric acid and
stimulate mucus and bicarbonate output; has antibacterial
effects on H. Pylori; useful in PUD; causes black tongue and
stools; increased bleeding time bismuth subsalicylate

19
Q

. Promotility Agents

A

Metoclopramide (Reglan)
therapeutic use: adjuncts to PPIs and H2 blockers for GERD; gastroparesis; antiemetic
mechanism of action: increases GI motility by stimulating ACh release from neurons in the enteric nervous system; increases LES pressure; metoclopramide also blocks D2 receptors
c. adverse effects: chronic use (>12 wk) may cause tardive dyskinesia

20
Q

HP eradication strategies

A

ex: PPI + clarithromycin + metronidazole;
PPI + clarithromycin + amoxicillin;
PPI + amoxicillin + metronidazole

advantages of three-drug regimen include better compliance, more efficacious, less antibiotic resistance

if a second course is required, the patient should receive a different antibiotic regimen

21
Q

NSAID-induced ulcers

A

standard regimens of H2As or PPIs or sucralfate if the NSAID is discontinued

PPIs if the NSAID is continued (better ulcer healing with PPIs)

22
Q

TREATMENT STRATEGIES FOR GERD

A
  1. Life-style changes (elevate head while sleeping, protein-rich
    meals, stop smoking, avoid alcohol)
  2. Use of antacids, alginic acid compounds, and/or OTC H2As
  3. Prescription H2As
  4. Prescription PPIs or higher dose H2As
  5. Surgery
  6. Prevent recurrence: PPIs, ranitidine (only H2A for erosive
    esophagitis)